Let’s Get Updated – Episode 1: An Introduction to Cardiovascular Physiology (UIA Vol. 24, No. 2)

Let’s Get Updated is an audio learning series that brings to life the key topics from Update in Anaesthesia—one topic at a time. Each episode guides you through a full reading of a selected topic, making it easy to listen and read along. Whether you’re preparing for exams or brushing up on essential concepts, this podcast is built for anaesthesia learners in all settings, especially low-resource environments. This is an independent educational project not affiliated with the World Federation of Societies of Anaesthesiologists (WFSA). Content is drawn from publicly available issues of Update in Anaesthesia. ~~~~~~~~~~ This episode features a full reading of “An Introduction to Cardiovascular Physiology” from Update in Anaesthesia, Volume 24, Number 2. Read along with the original article or simply listen in for a clear, guided walkthrough. Let’s get updated.

Episode Transcript

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Updates in Anaesthesia volume 24#2 An introduction to
cardiovascular Physiology by James Rogers introduction The

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cardiovascular system consists of the heart and two vascular
systems, the systemic and pulmonary circulations.
The heart pumps blood through these two vascular systems, the

(00:44):
low pressure pulmonary circulation in which gas
exchange occurs, and then the high pressure systemic
circulation which delivers bloodto individual organs, matching
supply to metabolic demand. Blood pressure and flow are

(01:10):
largely controlled by the autonomic nervous system and are
also influenced by surgery and anaesthetic drugs.
The Heart The heart comprises 4 chambers and is divided into a

(01:32):
right and left side, each with an atrium and a ventricle.
The Atria acts as reservoirs forvenous blood with some pump with
some pumping action to assist ventricular feeling.

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In contrast, the ventricles are the major pumping chambers
delivering blood to the pulmonary that is right
ventricle and systemic that is left ventricle circulations.
The left ventricle is conical inshape and has to generate

(02:19):
greater pressures than the rightventricle and so has a much
thicker and more muscular wall. 4 valves ensure that blood flows
only one way from Atria to ventricle, that is triscus speed

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and mitral valves and then to the atrial circulations, that is
pulmonary and aortic valves. The myocardium consists of
muscle cells which can contract spontaneously and pacemaker and

(03:01):
conducting cells which have specialised functions.
Electrophysiology of the heart. Myocardial contraction results
from a change in voltage across the cell membrane, that is
depolarization, which leads to an action potential.

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Although contraction may happen spontaneously, it is normally in
response to an electrical impulse.
This impulse starts in the sinoatrial that is SA node, a
collection of pacemaker cells located at the junction of the

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right atrium and superior venal cover.
These specialised cells depolarize spontaneously and
cause a wave of contraction to pass across the Atria.
Following atrial contraction, the impulse is delayed at the

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atrioventricular, that is, AV node located in the septal wall
of the right atrium. From here, histoporkinje fibres
allow rapid conduction of the electrical impulse via right and

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left branches, causing almost simultaneous depolarization of
both ventricles. Approximately 0.2 seconds after
the initial impulse has arisen in the sinoatrial node,

(05:01):
depolarization of the myocardialcell membrane causes a large
increase in the concentration ofcalcium within the cell, which
in turn causes contraction by a temporary binding between two

(05:22):
proteins, actin and myosin. The cardiac action potential is
much longer than that of skeletal muscle, and during this
time the myocardial cell is unresponsive to further

(05:44):
excitation, that is the refractory period, the
electrocardiogram ECG. The ECG measures changes in skin
electrical voltage stroke potential caused by electrical

(06:09):
currents generated by the myocardium.
The P wave reflects atrial depolarization, the QRS complex
ventricular depolarization, and the T wave ventricular

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repolarization. Repolarization is a process that
occurs in many cells where the electrical potential across the
cell membrane returns from the value during the action
potential to that of the restingstate, the resting potential.

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Although the ECG shows the heartrate and rhythm and can indicate
myocardial damage, it gives no information on the adequacy of
contraction. Normal electrical complexes can
exist in the absence of cardiac output, a state known as

(07:24):
pulseless electrical activity. Sorry, we should have talked
about the summary in the beginning of this topic, so
let's just talk about it now. Summary.
This article aims to provide an overview of the Physiology of

(07:48):
the cardiovascular system and its response to anaesthesia.
The next article in this sectiondeals with myocardial Physiology
in greater detail. So back to the topic cardiac

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output. Cardiac output Co is the product
of heart rate, HR and stroke volume.
SV. That is Co equals to HR times
SV. For a 70 kilogramme man.

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Normal values are HR equals 70 per minute and SV equals 70
mills giving a cardiac output ofabout 5 litres per minute.

(08:58):
The cardiac index is the cardiacoutput per square metre of body
surface area and normal values range from 2.5 to 4.0 litres per
minute per metre. Square heart rate is determined

(09:26):
by the rate of spontaneous depolarization at the sinuatrial
node. See article on myocardial
Physiology but can be modified by the autonomic nervous system.
The vagus nerve acts on the muscarinic receptors to slow the

(09:48):
heart, whereas the cardiac sympathetic fibres stimulate
beta hydrogenergic receptors andincrease heart rate.
Stroke volume is determined by three main factors, preload,

(10:13):
afterload, and contractility. Preload is the ventricular
volume at the end of diastole. An increased preload leads to an
increased stroke volume. Preload is mainly dependent on

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the return of venous blood from the body and is influenced by
changes in position, intrathoracic pressure, blood
volume and the balance of constriction and dilation, that
is, tone in the venous system. The relationship between

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ventricular end diastolic volumeand stroke volume is known as
Sterling's law, which states that the energy of contraction
of the muscle is related stroke proportional to the initial

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length of the muscle fibre. This can be graphically
illustrated by a series of styling curves shown in Figure 1
as volume at the end of diastole.
That is, end diastolic volume increases and stretches the

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muscle fibre, so the energy of contraction and stroke volume
increase until a point of overstretching when stroke
volume may actually decrease, asin the failing heart.

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Cardiac output will also increase or decrease in parallel
with stroke volume if there is no change in heart rate.
The curves show how the heart performs at different states of
contractility, ranging from the normal heart to one in

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cardiogenic shock. This is a condition where the
cardiac output is insufficient to maintain tissue perfusion.
Also shown is the curve for an increasing level of physical
activity, which requires A corresponding increase in

(13:00):
cardiac output. Next we get to Figure 1
describing Sterling's law. It says the curves A&B
illustrate the rise in cardiac output which increases in
ventricular and diastolic volume, that is preload in the

(13:22):
normal heart. Note that with an increase in
contractility, there is a greater cardiac output for the
same ventricular end diastolic volume in the diseased heart,
that is C&D, that is heart failure and in cardiogenic
shock. Cardiac output is less and falls

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if ventricular end diastolic volume rises to high levels as
in heart failure or overload after load.
Is the resistance to ventricularejection assuming the aortic

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valve is normal. This is caused by the resistance
to flow in the systemic circulation and is the systemic
vascular resistance that is SVR.The resistance is determined by
the diameter of the atrios and pre capillary sphincters.

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The narrower or more constrictedthe higher the resistance.
The level of SVR is controlled by the sympathetic system, which
controls the tone of the muscle in the wall of the arterial and
hence the diameter. The resistance is measured in

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units of dying second per centimetre raised to the power
of 5. A series of sterling curves with
differing after loads is shown in Figure 2, demonstrating a

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fall in stroke volume as after load increases.
The relationship between systemic vascular resistance and
the control of arterial pressureis discussed below.

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We get to Figure 2 talking aboutthe relationship between stroke
volume and after load. A series of curves illustrate
the effects of increasing after load on systemic vascular
resistance. As after load increases, the

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patient moves to a lower curve with its lower stroke volume for
the same ventricular end diastolic volume.
That is, preload. Contractility describes the

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ability of the myocardium to contract in the absence of any
changes in preload or afterload.In other words, it is the power
of the cardiac muscle. The most important influence on

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contractility is the sympatheticnervous system.
Beta adrenergic receptors are stimulated by norephinephrine,
that is no adrenaline released from nerve endings and
contractility increases. A similar effect is seen with

(17:16):
circulating epinephrine, that isadrenaline and drugs such as
ephedrine, digoxin, and calcium.Contractility is reduced by
acidosis, myocardial ischemia and the use of beta blocking and

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anti arrhythmic agents. Cardiac output will change to
much changing metabolic demands of the body.
The outputs of both ventricles must be identical and also equal

(18:06):
the volume return of blood from the body.
The balancing of cardiac outputsand venous return is illustrated
using. During the response to exercise,
blood vessels dilate in exercising muscle groups because

(18:28):
of increased metabolism and blood flow increases this
increase. This increases venous return and
right ventricular preload. Consequently, more blood is
delivered to the left ventricle and cardiac outputs increases.

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There will also be increased contractility and heart rate
from the sympathetic activity associated with exercise,
further increasing cardiac output to meet tissue
requirements. Control of heart rate.

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The heart will beat independently of any nervous or
hormonal influences. The spontaneous rhythm of the
heart, called intrinsic automaticity, can be altered by
nervous impulses or by circulatory substances like

(19:44):
epinephrine. The muscle fibres of the heart
are excitable cells like other muscle or nerve cells, but have
a unique property each cell in the heart.
Will spontaneously contract at aregular rate because the

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electrical properties of the cell membrane spontaneously
alter with time and regularly depolarize.
Depolarization means that the electrical gradient across the
cell membrane becomes less negative and then reverses,

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causing muscle contraction or passage of a nervous impulse.
Muscle fibres from different parts of the heart have
different rates of spontaneous depolarization.
The cells from the ventricle arethe slowest and those from the

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Atria are faster. The coordinated contraction of
the heart is produced because the cells with the fastest rate
of depolarization capture the rest of the heart muscle cells.

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These cells with the fastest rate of depolarization are in
the sinoatrial node, that is, SAnode, the pacemaker of the heart
found in the right atrium. As the SA node depolarize
depolarizes, a wave of electrical activity spreads out

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across the atrium to produce atrial contraction.
Electrical activity then passes through the atrioventricular
node that is AV node and throughinto the ventricles via the
parkingeer fibres in the bundle of his to produce a ventricular

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contraction. If there is any disease of the
conducting system of the heart, then this process may be
interfered with and the heart rate altered.
If for example, there is diseaseof the AV node, then there is an

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electrical block between the Atria and the ventricles.
The ventricles will beat with their own inherent rhythm which
is much slower, usually 30 to 50beats per minute.

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Anaesthetic drugs like halothanemay depress the rate of
depolarization of the SA node, and the AV node may become the
pacemaker of the heart. When this occurs, it is
frequently termed nodal or junctional rhythm.

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This automatic rhythm of the heart can be altered by the
autonomic nervous system. The sympathetic nervous system
supply to the heart leaves the spinal cord at the 1st 4
thoracic vertebrae and supplies most of the muscle of the heart.

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Stimulation via the cardiac betaone receptors causes the heart
rate to increase and beat more forcefully.
The vagus nerve also supplies the Atria and stimulation causes

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the heart rate to decrease, thatis bradycardia.
Surgical procedures can cause vagal stimulation and produce
severe bradycardia. Examples include pulling on the

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mesentry of the boreal, anal dilatation, or pulling on the
external muscles of the eye. Under normal conditions, the
vagus nerve is the more important influence on the

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heart. This is especially noticeable in
athletes who have slow heart rates.
There are nervous reflexes that affect heart rate.
The aference, IE going to the brain, are nerves in the wall of

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the Atria or aorta that respond to stretch.
The aorta contains high pressurereceptors.
When the blood pressure is high,these cause reflux slowing of
the heart to reduce the cardiac output and the blood pressure.

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Similarly, when the blood pressure is low, the heart rate
increases as in shock. Similar pressure receptors are
found in the Atria. When the Atria distend, as in
heart failure or overtransfusion, there is a

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reflex increase in the heart rate to pump the extra blood
returning to the heart. When there is a sudden reduction
in the pressure in the Atria, the heart slows.

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This is called the brain bridge reflex and is the cause for the
marked bradycardia sometimes seen during spinal anaesthesia.
It is best treated by raising the legs to increase the venous

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return. Early administration of a
cardioaccelerator such as ephedrine or epinephrine is
recommended if there is no immediate response to this
manoeuvre. Circulatory substances can also

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affect the heart rate. Catecholamines like epinephrine
are released during stress and will cause an increase in heart
rate. Drugs are another common cause
of change in the heart rate and and most anaesthetic drugs can

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do this. Halothane affects the SA node
and will also depress the force of contraction of the heart of
the heart. Isofluorine, by contrast, has
little if direct effect on the heart but causes peripheral

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vasodilation of the blood vessels.
This will then decrease the blood pressure and hence produce
a reflex tachycardia. As explained above,
administration of greater than one MVC of desfluorine or

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isofluorine may increase sympathetic outflow and so
increase heart rate transiently and acutely.
This does not happen with sevo fluorine.
Ketamine causes stimulation of the sympathetic nervous system

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and therefore produces a tachycardia.
Other circulating substances mayalso affect the heart rate,
acting indirectly through the autonomic nervous system.
For example, increased blood concentrations of carbon dioxide

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will cause stimulation of the sympathetic nervous system and
tachycardia, and this is an important sign of respiratory
failure. The systemic circulation The

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systemic blood vessels are divided into arteries,
arterioles, capillaries, and veins.
Arteries supply blood to the organs at high pressure, whereas
arterioles are smaller vessels with muscular walls, which allow

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direct control of flow through each capillary bed.
Capillaries consist of a single layer of endothelial cells, and
the thin walls allow exchange ofnutrients between blood and
tissue. Veins return blood from the

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capillary beds to the heart and contains 70% of the circulating
blood volume, in contrast to 15%in the arterial system.
Veins act as a reservoir and venous tone is important in

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maintaining the return of blood to the heart, for example, in
severe haemorrhage when sympathetic stimulation causes
venous constriction. Blood flow.

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The relationship between flow and driving pressure is given by
the high gain post well formula.This states that flow rates in a
tube is proportional to driving pressure times radius raised to

(31:12):
the power of 4 divided by lengthtimes viscosity.
We take it again. Flow rates in a tube is directly
proportional to driving pressuretimes radius raised to the power
of 4 divided by length times viscosity.

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In blood vessels, flow is posatile rather than continuous,
and viscosity varies with flow rates, so the formula is not
strictly applicable. However, it illustrates an

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important point. Small changes in the radius
result in large changes in flow rates in both arterioles and
capillaries. Changes in flow rates are
brought about by changes in toneand therefore vessel radius.

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Viscosity describes the tendencyof a fluid to resist flow.
At low flow rates, the red bloodcells stick together increasing
viscosity and remain in the centre of the vessel.

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The blood closest to the vessel wall, which that is, which
supplies the side branches, therefore has a lower
hematocrit. This process is known as plasma
scheming. Viscosity is reduced in the

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presence of anaemia and the resulting increase flow rate
helps maintain oxygen delivery to the tissues.
Control of the systemic circulation.

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Arteriola tone determines blood flow to the capillary beds.
A number of factors influenced Arteriola tone, including
autonomic control, circulating hormones, Endotherium derive

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factors and the local concentration of metabolites.
Autonomic control is largely by the sympathetic nervous system,
which supplies all vessels except the capillaries.

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Sympathetic fibres arise from the thoracic and lumbar segments
of the spinal cord. These are under the control of
the Vasomoto centre in the medulla, which has distinct
vasoconstrictor and vasodilator areas.

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Although there is a baseline sympathetic discharge to
maintain vascular tone, increased stimulation effects
some organs more than others. This tends to redistribute blood
from skin, muscle and gut to thebrain, heart and kidney.

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Increased sympathetic discharge is one of the responses to
hypovolemia. For example, in severe blood
loss with the effect of protecting blood supply to the
vital organs, the predominant sympathetic influence is

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vasoconstriction via alpha adrenergic receptors.
However, the sympathetic system also causes vasodilation via
beta adrenergic and cholinergic receptor stimulation, but only

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in skeletal muscle. This increased blood flow to
muscle is an important part of the fight or flight reaction
when exercise is anticipated. Next we go to Figure 3, talking

(36:20):
about the effects of sympatheticnervous stimulation on vascular
resistance in different organs. Note that for the same
sympathetic stimulation, the resistance is higher in skin.
The resistance is higher in skincirculating hormones such as

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epinephrine and angiotensin. 2 are potent vasoconstrictors, but
they probably have little effecton acute cardiovascular control.
In contrast, endothelium derivedfactors play an important role

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in controlling local blood flow.These substances are either
produced or modified in the vascular endothelium and include
prostacyclin and nitric oxide, both potent vasodilators.

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An accumulation of metabolites such as carbon dioxide,
potassium, hydrogen, adenosine and lactate causes vasodilation.
This response is probably an important mechanism of auto

(37:59):
regulation, the process whereby blood flow through an organ is
controlled locally and remains constant over a wide range of
perfusion. Pressure autoregulation is a
particular feature of the cerebral, cerebral, and renal

(38:24):
circulations. Control of arterial pressure
Systemic arterial pressure is controlled closely in order to
maintain tissue perfusion. The mean arterial pressure that

(38:48):
is MAP takes account of pulsatide blood flow in the
arteries and is the best measureof perfusion pressure to an
organ. MAP is defined as diastolic
arterial pressure plus 1/3 of the pulse pressure, where the

(39:12):
pulse pressure is the differencebetween systolic and diastolic
arterial pressure. MAP is the product of cardiac
output and systemic vascular resistance and can be thought of
as an analogous to Ohm's law, that is, V equals IR.

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In other words, MAP is equals toCo times SVR.
That is, mean arterial pressure is equal to cardiac output times
systemic vascular resistance if cardiac output falls, for

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example when venous return decreases in hypovolemia.
MAP will also fall unless there's a compensatory rise in
SVR by a vassal constriction of the arterioles.
This response is mediated by baroreceptors, which are

(40:28):
specialised sensors of pressure located in the chaotic sinus
aniotic arc and connected to thevasomoto centre in the
brainstem. A fall in blood pressure causes
reduced stimulation of the Burrow receptors and consequent

(40:52):
reduced discharge from the Burrow receptors to the vasomoto
centre. This causes an increase in
sympathetic discharge leading tovasoconstriction, increased
heart rate and contractility, and secretion of epinephrine.

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Conversely, rises in blood pressure stimulates the
baroreceptors, which leads to increased parasympathetic
outflow to the heart via branches of the vagus nerve,
causing slowing of the heart. There is also reduced
sympathetic stimulation to the peripheral vessels causing

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vasodilation. Baroreceptor responses provide
immediate control of blood pressure.
If hypertension is prolonged, other mechanisms start to
operate, such as the release of angiotensin 2 and aldosterone

(42:03):
from the kidneys and adrenal glands, which leads to salt and
water being retained in the circulation.
The Vasalva manoeuvre is a simple test of the baroreceptor
reflex. The patient tries to breathe out

(42:27):
forcefully against a closed larynx, resulting in an
increased intrathoracic pressure.
These causes decreased venous return, cardiac output and a
fall in blood pressure, leading to reduced barrel receptor

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discharge to the vasometer centre.
This then causes peripheral vasoconstriction and an increase
in heart rate, which is the normal response.
This has the effect of maintaining systolic pressure,

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although the pulse pressure is reduced due to vessel
constriction. Cardiovascular responses to
anaesthesia. All anaesthetic agents have a

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direct depressant effect on the myocardium.
Therefore they reduce myocardialcontractility and may also
reduce sympathetic stimulation of the vascular system.
The result is a decreased cardiac output accompanied by

(43:56):
vasodilation causing hypertension.
This fall in blood pressure can compromise perfusion of vital
organs, especially at induction of anaesthesia in the
hypovolemic patients. In contrast, agents such as

(44:20):
ketamine and ether increase sympathetic activity, which
opposes the direct depressant effect.
These cardiac output and blood pressure sorry.
Thus, cardiac output and blood pressure are maintained despite

(44:41):
the direct myocardial depressantaction.
Volatile and aesthetic agents reduce discharge from the
sinuatrial node. This can lead to junctional
rhythms when the atrioventricular node takes over

(45:02):
as pacemaker associated with an absent P wave on the ECG.
Local anaesthetic agents depressconduction of the cardiac
impulse. This effect can be therapeutic,

(45:25):
for example in the treatment of ventricular arrhythmias with
lidocaine. Controlled ventilation in a
paralysed patient has many effects on the cardiovascular
system. Firstly, it increases

(45:46):
intrathoracic pressure which reduces venous return and
preload, causing a fall in cardiac output.
Secondly, changes in the partialpressure of carbon dioxide
resulting from changes in ventilation will also have

(46:09):
cardiovascular effects. A low PA CO2, which commonly
occurs during controlled ventilation, causes peripheral
vasoconstriction by a direct effect.

(46:29):
This increases systemic vascularresistance, increases after
load, and can result in a fall in cardiac output if it also
causes cerebral vasoconstriction, reducing
cerebral blood volume. A high PO CO2 usually occurs in

(46:57):
the anaesthetized patient duringspontaneous breathing and causes
vasodilation and increased sympathetic activity, leading to
increased cardiac output. However, the heart will be more
likely to develop arrhythmias, particularly when using volatile

(47:20):
agents. Spinal and epidural anaesthesia
blocks sympathetic nerves as well as sensory and motor
nerves. This can lead to marked
hypertension due to arterial andvenous dilation because of the

(47:42):
sympathetic nerves to the lower extremities are blocked.
Cardiac sympathetic nerve fibreswhich arise from the high
thoracic spinal cord may also beblocked, allowing an unopposed
vagal action on the heart. In this case, there will not be

(48:08):
an appropriate increase in heartrate and blood pressure will
fall further.